Circ_0025039 acts an oncogenic role in the progression of non-small cell lung cancer through miR-636-dependent regulation of CORO1C.

Non-small cell lung cancer remains the leading cause of cancer-related death worldwide. Circular RNA plays vital roles in NSCLC progression. This study is designed to reveal the role of circ_0025039 in NSCLC cell malignancy. The RNA expression of circ_0025039, microRNA-636 (miR-636), and coronin 1C was detected by quantitative real-time polymerase chain reaction. Protein expression was checked by Western blot analysis or immunohistochemistry assay. Cell proliferation, migration, invasion, tube formation ability, sphere formation capacity, and apoptosis were investigated by cell counting kit-8, 5-Ethynyl-29-deoxyuridine, transwell assay, tube formation assay, sphere formation assay, and flow cytometry analysis, respectively. Mouse model assay was conducted to reveal the effect of circ_0025039 silencing on tumor formation in vivo. The interaction between miR-636 and circ_0025039 or CORO1C was identified through dual-luciferase reporter and RNA pull-down assays. The expression of circ_0025039 and CORO1C was significantly increased, while miR-636 was decreased in NSCLC tissues and cells compared with controls. Circ_0025039 depletion repressed NSCLC cell proliferation, migration, invasion, tube-forming capacity, and sphere formation ability, but induced cell apoptosis. The neoplasm formation was repressed after circ_0025039 silencing. Additionally, circ_0025039 acted as a sponge for miR-636, which was found to target CORO1C. Importantly, the contribution of circ_0025039 to NSCLC progression was mediated by miR-636/CORO1C axis. Circ_0025039 silencing repressed NSCLC malignant progression by reducing CORO1C expression through miR-636, showing the possibility of circ_0025039 as a therapeutic target for NSCLC.

Diagnosis and treatment for a case of Legionella longbeachae severe pneumonia and literature review. / 1ä¾‹é•¿æ»©å†›å›¢èŒæ€§é‡ç—‡è‚ºç‚Žè¯Šæ²»åˆ†æžåŠæ–‡çŒ®å¤ä¹ .

As a type of Legionella bacteria, Legionella longbeachae bacteria can lead to very rare legionella disease case in China with clinical characteristics, such as no typical early clinical symptoms, strong toxicity, high mortality, and not easy to detect by conventional etiology. A case of severe pneumonia caused by Legionella longbeachae infection was confirmed by bronchoalveolar lavage fluid pathogen metagenomics, and the patient's condition was improved after targeted anti-infection treatment. At present, our understanding in Legionella longbeachae severe pneumonia is limited. The diagnosis and treatment process of the patient with severe pneumonia of Legionella longbeachaeis retrospectively analyzed and the relevant literature was reviewed to provide the experience for its future diagnosis and treatment.

Syntenin overexpression in human lung cancer tissue and serum is associated with poor prognosis.

BACKGROUND: Lung cancer is the major malignant tumour. The present study was conducted to determine the expression level of syntenin in lung cancer tissues and serum from lung cancer patients and to explore its clinical significance. METHODS: Syntenin expression levels were determined in paraffin-embedded lung cancer tissue specimens (n = 191) using immunohistochemistry. The mRNA expressions of syntenin in fresh lung cancer tissues and the paracancerous tissues were examined by RT-qPCR (n = 25). Syntenin and VEGF expression levels were measured in serum from patients with lung cancer (n = 60) and control subjects (n = 30) using ELISA. The associations between syntenin and the clinicopathological features or prognosis in 191 patients with lung cancer were analysed. The correlation between the syntenin and VEGF levels in serum from 60 lung cancer patients was analysed. RESULTS: The expression levels of syntenin were significantly higher in lung cancer tissues than in paracancerous tissues based on immunohistochemistry and RT-qPCR, and elevated syntenin expression was significantly associated with tumour size (P = 0.002), TNM stage (P = 0.020), tumour distant metastasis (P = 0.033), overall survival (OS) (P = 0.002) and progression-free survival (PFS) (P = 0.001). Multivariate analysis revealed that increased expression of syntenin was an independent risk factor for OS (P = 0.006) and PFS (P < 0.001) in lung cancer patients. The expression levels of syntenin and VEGF in serum from lung cancer patients were higher than those from control subjects (P < 0.001, P < 0.001, respectively), and their expression levels were positively correlated (r = 0.49, P < 0.001). CONCLUSIONS: Syntenin expression is upregulated in lung cancer patients, and its serum expression level is positively correlated with VEGF. Moreover, syntenin overexpression was correlated with poor prognosis in patients with lung cancer.

miR-497 over-expression inhibits epithelial-mesenchymal transition in lung cancer A549 cells by targeting cyclin E1 / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨过表达miR-497靶向细胞周期蛋白E1（cyclin E1，CCNE1）对肺癌A549细胞上皮间质转化（epithelial-mesenchymal transition，EMT）的影响。方法：常规培养人肺癌A549细胞，细胞实验分为正常组（不加干预）、对照组（转染miR-497 mimics-NC）、实验组（转染miR-497 mimics）。采用Transwell小室实验、免疫荧光染色、qPCR、Western blotting法分别检测各组细胞迁移和侵袭能力、蛋白间质标志物α-SMA和上皮标志物E-cadherin的表达、miR-497和CCNE1的表达水平，荧光素酶基因基因报告实验验证miR-497和CCNE1的靶向关系。结果：与对照组和正常组相比，实验组A549细胞迁移和侵袭的数量明显减少（均P<0.05），细胞的间质标志物α-SMA的绿色荧光强度明显减弱[（36.95±5.81） vs （98.69±2.36）、（97.94±2.63），均P<0.05]，上皮标志物E-cadherin的绿色荧光强度明显增强[（388.41±10.93） vs （100.95±6.37）、（102.55±3.18），均P<0.05]，miR-497的表达明显升高（均P<0.05），CCNE1的表达均明显下降（均P<0.05）。miR-497能够靶向调控CCNE1的表达。结论：在肺癌A549细胞中miR-497能够靶向调控CCNE1的表达，上调miR-497的表达后能明显抑制A549细胞迁移和侵袭能力，影响EMT相关蛋白的表达。

[Inhibition of pulmonary nuclear factor -ΚB and tumor necrosis factor -α expression by diallyl sulfide in rats with paraquat poisoning].

OBJECTIVE: To investigate the mechanism of anti-inflammatory effect of diallyl sulfide (DAS) in protection against acute lung injury (ALI) in rats with paraquat poisoning. METHODS: Eighty male Wistar rats were randomly divided into four groups, namely: control group, model group, dexamethasone (DXM) treatment group, and DAS treatment group, with 20 rats in each group. The model of paraquat poisoning was reproduced by single does of 70 mg/kg given by gavage, while the same volume of normal saline (NS) was given in same manner in control group. 100 mg/kg of DAS, the same volume of NS, or 1 mg/kg DXM injection were given respectively in DAS treatment group, model group, or DXM treatment group intraperitoneally after exposure to paraquat, once a day for 14 days. Five rats in each group were sacrificed at 1, 3, 7, 14 days, respectively. The inferior lobe of right lung was harvested, and the degree of lung injury was observed with hematoxylin and eosin (HE) staining under optical microscope; the upper lobe of right lung was used to determine the lung wet/dry weight (W/D) ratio and for evaluation of the degree of pulmonary edema. The expression of nuclear factor -ΚB (NF-ΚB) in the middle lobe of right lung was assessed with immunohistochemistry. The expression of tumor necrosis factor -α ( TNF-α ) mRNA in the left lung was determined with the reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: (1) The pulmonary structure in control group was found to be intact. However, in the model group there were progressive pathological changes in lung, including marked edema and thickening of alveolar walls, collapse of alveoli, infiltration of inflammatory cells, alveolar wall, and obvious bleeding in the local lung tissue, and formation of transparent membrane in alveolar space. Less infiltration of inflammatory cells and no obvious destruction were found in alveolar structure in the DAS and DXM treatment groups. (2) Lung W/D ratio: lung W/D ratio of model group was apparently higher than that in control group at every time point, and peaking on the 3rd day ( 6.15 ± 0.54 vs. 4.15 ± 2.10, P < 0.05 ), and the ratio of lung W/D of DAS and DXM treatment groups was obviously lower than that in model group at every time point, especially on the 3rd day (3.99 ± 1.26, 4.30 ± 0.70 vs. 6.15 ± 0.54, both P < 0.05), but there was no significant difference between DAS and DXM treatment groups in this regard. (3) The immunocytochemistry analysis revealed minimal NF-ΚBp65 expression in the cell nuclei of the control group, while extensive NF-ΚBp65 expression was found in model group. Minimal NF-ΚBp65 positive expression in the cytoplasm and even less positive expression in the nucleus was found in the DAS and DXM treatment groups, and integral A value was significantly lower in the DAS and DXM treatment groups than that of the model group, especially on the 3rd day [(17.98 ± 0.06 )× 107, (18.53 ± 0.04) × 107 vs. (28.85 ± 0.61) × 107, both P < 0.01], but there was no significant difference between DAS and DXM treatment groups. (4) It was shown by RT-PCR that the expression of TNF-α mRNA in lung tissue of the model group was significantly higher than that in the control group on the 3rd day (gray value: 3.63 ± 0.62 vs. 0.51 ± 0.13, P < 0.05 ). The expression of TNF-α mRNA in lung tissue was significantly decreased in DAS and DXM treatment groups compared with model group ( gray value: 2.49 ± 0.57, 2.02 ± 0.26 vs. 3.63 ± 0.62, both P < 0.05 ), but there was no significant difference between DAS and DXM treated groups. CONCLUSIONS: Treatment with an intraperitoneally injection of DAS is capable of attenuate the extent of PQ-induced ALI in rats by alleviating pulmonary edema, inhibiting the expression of NF-ΚB and TNF-α in lung tissue, and ameliorating pathological changes in lung tissue.